三氮唑通过上调 p38 磷酸化抑制肝癌细胞活力并靶向作用于 p-ERK1/2 和 Akt 蛋白表达的激活。

Inhibition of Liver Cancer Cell Viability by Triazole through Up-regulation of p38 Phosphorylation and Targeting the Activation of p-ERK1/2 and Akt Protein Expression.

机构信息

Interventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China.

出版信息

Dokl Biochem Biophys. 2024 Jun;516(1):66-72. doi: 10.1134/S1607672923600525. Epub 2024 May 3.

Abstract

The present study was aimed to explore the effect of triazole on growth and viability of liver cancer cells. Cell growth was examined using the MTT test and expression of several proteins was assessed by western blotting assay. The Matrigel-coated Transwell assay was employed to examine the infiltration of cells. The data from MTT assay showed that MHCC97H and H4TG liver cancer cell viability was inhibited by triazole in a concentration-dependent manner. After treatment with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole, the rate of H4TG cell viability was decreased to 96, 73, 58, 39, 29, and 28%, respectively. Treatment of MHCC97H cells with 0.5, 1.0, 2.0, 4, 8, and 16 µM doses of triazole resulted in a reduction in cell viability to 94, 70, 53, 35, 22, and 21%, respectively. Triazole treatment also led to a significant reduction in MHCC97H cell invasiveness compared to the control cells. In MHCC97H cells treated with triazole, there was a noticeable decrease in the levels of p-ERK1/2, and p-Akt protein expression. Treatment of MHCC97H cells with triazole resulted in a prominent increase in p-p38 level. In summary, triazole inhibits growth and viability of liver cancer cells through targeting the activation of p-ERK1/2 and Akt proteins. Therefore, triazole may be investigated further as a therapeutic agent for the treatment of liver cancer.

摘要

本研究旨在探讨三氮唑对肝癌细胞生长和活力的影响。通过 MTT 试验检测细胞生长，通过 Western blot 试验评估几种蛋白质的表达。采用 Matrigel 包被的 Transwell 试验检测细胞浸润。MTT 试验结果显示，三氮唑以浓度依赖性方式抑制 MHCC97H 和 H4TG 肝癌细胞活力。用 0.5、1.0、2.0、4、8 和 16 µM 剂量的三氮唑处理后，H4TG 细胞活力率分别降至 96%、73%、58%、39%、29%和 28%。用 0.5、1.0、2.0、4、8 和 16 µM 剂量的三氮唑处理 MHCC97H 细胞后，细胞活力分别降至 94%、70%、53%、35%、22%和 21%。三氮唑处理还导致 MHCC97H 细胞侵袭性与对照细胞相比显著降低。用三氮唑处理 MHCC97H 细胞后，p-ERK1/2 和 p-Akt 蛋白表达水平明显下降。用三氮唑处理 MHCC97H 细胞导致 p-p38 水平显著升高。总之，三氮唑通过靶向抑制 p-ERK1/2 和 Akt 蛋白的激活来抑制肝癌细胞的生长和活力。因此，三氮唑可能作为治疗肝癌的治疗剂进一步研究。